Posted by Marty on August 14, 2008, at 12:12:32
In reply to Re: Bifeprunox not approved, posted by Jeroen on August 14, 2008, at 10:44:17
"along with SLV313, aripiprazole and SSR-181507 combines minimal D2 receptor agonism with 5-HT receptor agonism.[1]"
There's other drugs in the pipeline that works the same way Bifeprunox does. And that fact should have weighted in when the FDA refused to approve it.
Didn't searched it out, but I think the way it work as an partial agonist (vs antagonist) is that it stimulate the receptor to a less extend that the endogenous neurotransmitter (dopamine & serotonin) and so when they occuping the receptor the endogenous can't: they are competitive and the net effect is less stimulation than without the med at those receptor BUT somehow more than other antagonistic antipsychotics. When I say 'more' I think it should have something to do with what I would call the "Carrier Signal" or "No activity level".. I dont know the scientific term for that. But let's say those meds make sure you don't have too much dopaminergic (D2) activity but always a little.
Very interesting stuff! I should research this as I'm sure I'm partly wrong about the "Carrier Signal" thing. It should have something to do with LTP or better/constant very weak projection improvement that does the difference for schizophrenic.
If someone knows better than me I'd like to have an explanation.
/\/\arty
poster:Marty
thread:846140
URL: http://www.dr-bob.org/babble/20080814/msgs/846167.html